Acute Coronary Syndromes (ACS) are a major cause of mortality in Western countries. The key event in an overwhelming number of these cases is platelet thrombus formation. Consequently, there is strong interest in the development of safe and effective anti-thrombotic agents. Numerous agents have been developed that target the platelet activation cascade or prevent fibrinogen-mediated platelet-platelet aggregation (GPIIb/IIIa inhibitors). These approaches have produced some encouraging results. However, direct inhibition of the very first step in thrombus formation, namely, formation of the initial platelet monolayer, has received comparatively little attention to date. Platelet rolling over exposed subendothelium at sites of vascular injury is a crucial initiating step in hemostasis and thrombosis. This process depends critically on the interaction of platelet-receptor glycoprotein Ibα (GpIbα) and plasma-protein von Willebrand Factor (vWF). GpIbα not only plays a role in the adhesion to vWF, but also triggers the platelet into an activated state.